Blount Disease (Tibia Vara)

Blount disease (tibia vara) is a developmental growth disorder characterized by suppressed growth of the posteromedial proximal tibial physis, resulting in progressive varus angulation, internal tibial torsion, and procurvatum of the tibia. The medial growth plate shows abnormal cartilage development with disorganized chondrocyte columns, fibrocartilage formation, and eventually bony bridge formation in advanced cases. Excess mechanical force on the medial physis (obesity, early walking, constitutional varus) is thought to play a key role.

Three forms are recognized: infantile (onset before age 4, often bilateral, more common in obese children of African descent), juvenile (4–10 years), and adolescent (>10 years, usually unilateral, strong association with morbid obesity). Risk factors include obesity, early walking (<10 months), African ancestry, and family history. Differentiating infantile Blount disease from physiologic genu varum is critical: physiologic varum resolves spontaneously by age 2, while Blount progresses. Drennan's metaphyseal-diaphyseal angle >11° on standing radiograph favors Blount disease.

Langenskiöld classification stages I–VI describe progression of medial physeal changes (irregularity, depression, beaking, fragmentation, bridge formation). Treatment is stage-dependent. Bracing (knee-ankle-foot orthosis, KAFO) for stages I–II in children <3 years has variable success. Proximal tibial valgus osteotomy is required for stages III–VI or persistent deformity, with goal of restoring mechanical axis and correcting tibial torsion. In adolescents, hemiepiphysiodesis (guided growth with tension band plates) corrects mild deformity if growth remains. Bony bridge resection with interposition is needed for advanced infantile disease with established physeal bar. Weight loss and orthopedic monitoring are crucial for all forms.